Abstract
We observed the effects of endostar on the radiosensitivity of pulmonary adenocarcinoma A549 cells and found that endostar inhibited A549 cell growth under normoxia and hypoxia in time and dose-dependent manners; the D0 and Dq values in control and endostar groups were (1.36 and 1.30) versus (1.019 and 1.015) under normoxia and (1.693 and 1.39) versus (2.453 and 1.026) under hypoxia, respectively; SER was 1.04 under normoxia and 1.22 under hypoxia in endostar group; under normoxia, the apoptosis rates in control, radiotherapy, endostar and combination groups were 15.9 ± 0.57%, 42.7 ± 0.37%, 19.9 ± 0.48%, and 41.5 ± 0.38%, respectively, with no significant difference between combination and radiotherapy groups; there was significant difference in G2/M phase cells between combination and radiotherapy groups (P = 0.028); under hypoxia, the apoptosis rates in the four groups were 16.7 ± 0.67%, 30.1 ± 0.95%, 26.7 ± 0.62%, and 36.3 ± 0.71%, respectively, with significant difference between combination and radiotherapy groups; G2/M phase cells were higher in combination group than radiotherapy group (P = 0.000); G2/M phase cells were higher in hypoxic combination group than in normoxic combination group (P = 0.003). Based on these results, we conclude that under hypoxia, endostar can enhance the radiosensitivity of A549 cells through G2/M arrest.
Highlights
Lung cancer is one of the most common carcinoma in China
After A549 cells were treated with endostar of various concentrations for different durations under normoxia and hypoxia, endostar showed the inhibition effect on A549 cells compared with control groups (Tables 1 and 2)
A549 cells were treated with endostar of 7 different concentrations under normoxia and hypoxia, respectively, for 24–72 h, and the cell survival curve was drawn based on the results determined by MTT assay
Summary
Lung cancer is one of the most common carcinoma in China. Radiotherapy is a main therapeutic method for lung cancer, especially for locally advanced non-small-cell lung cancer (stage IIIA-B) [1]. Precise radiotherapy fails to improve the long-term survival rate of patients with malignant tumors. This may be that local radiotherapy cannot control tumor metastasis and recurrence, and there are a large number of radioresistant cells in tumor tissue. Finding an effective radiosensitizer to improve therapeutic effects has become a focus in tumor radiotherapy. Endostatin, a natural protein in animals, was first obtained from the supernatant of mouse hemangioendothelioma cell culture. Natural Endostatin is very unstable with shorter half life and lower biological activity. Jain [4] have found that angiogenesis inhibitors can make tumor blood vascular system normalize, relieving tumor hypoxia. Casanovas [6] recently reports that the radiosensitizing effect of angiogenesis inhibitors may be not associated with blood vascular system normalization. In order to further explore the radiosensitizing effects of endostar and its mechanism, we observed the effects of endostar on human pulmonary adenocarcinoma cell line A549 under normoxia and hypoxia in vitro, respectively
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